Results 151 to 160 of about 1,642,696 (345)

Measurement of the Activity of Wildtype and Disease-Causing ALPK1 Mutants in Transfected Cells With a 96-Well Format NF-κB/AP-1 Reporter Assay

Bio-Protocol
Alpha-protein kinase 1 (ALPK1) is normally activated by bacterial ADP-heptose as part of the innate immune response, leading to the initiation of downstream signalling events that culminate in the activation of transcription factors such as NF-κB and AP ...
Tom Snelling
doaj   +1 more source

A bioinformatics screen identifies TCF19 as an aggressiveness‐sustaining gene in prostate cancer

Molecular Oncology, EarlyView.
Gene expression meta‐analysis in multiple prostate cancer patient cohorts identifies Transcription factor 19 (TCF19) as an aggressiveness‐sustaining gene with prognostic potential. TCF19 is a gene repressed by androgen signaling that sustains core cancer‐related processes such as vascular permeability or tumor growth and metastasis.
Amaia Ercilla, Jana R. Crespo, Saioa Garcia‐Longarte, Marta Fidalgo, Sara del Palacio, Natalia Martin‐Martin, Onintza Carlevaris, Ianire Astobiza, Sonia Fernández‐Ruiz, Marc Guiu, Laura Bárcena, Isabel Mendizabal, Ana M. Aransay, Mariona Graupera, Roger R. Gomis, Arkaitz Carracedo   +15 more
wiley   +1 more source

Quantitative Measurement of the Kinase Activity of Wildtype ALPK1 and Disease-Causing ALPK1 Mutants Using Cell-Free Radiometric Phosphorylation Assays

Bio-Protocol
ALPK1 is an atypical protein kinase that is activated during bacterial infection by ADP-heptose and phosphorylates TIFA to activate a cell signaling pathway.
Tom Snelling
doaj   +1 more source

PHOSPHORYLATIVE AND NON-PHOSPHORYLATIVE OXIDATION IN ACETOBACTER SUBOXYDANS [PDF]

Journal of Biological Chemistry, 1952
Vernon H. Cheldelin, Tsoo E. King
openaire   +2 more sources

Modeling hepatic fibrosis in TP53 knockout iPSC‐derived human liver organoids

Molecular Oncology, EarlyView.
This study developed iPSC‐derived human liver organoids with TP53 gene knockout to model human liver fibrosis. These organoids showed elevated myofibroblast activation, early disease markers, and advanced fibrotic hallmarks. The use of profibrotic differentiation medium further amplified the fibrotic signature seen in the organoids.
Mustafa Karabicici, Soheil Akbari, Ceyda Caliskan, Canan Celiker, Ozden Oz, Leman Binokay, Gökhan Karakulah, Serif Senturk, Esra Erdal   +8 more
wiley   +1 more source

Studies on the oxidative phosphorylation and acidic secretion of the gastric mucosa and influence of the autonomic denervation on them

, 1958
Tetsuya Kikuchi
openalex   +2 more sources

PYCR1 inhibition in bone marrow stromal cells enhances bortezomib sensitivity in multiple myeloma cells by altering their metabolism

Molecular Oncology, EarlyView.
This study investigated how PYCR1 inhibition in bone marrow stromal cells (BMSCs) indirectly affects multiple myeloma (MM) cell metabolism and viability. Culturing MM cells in conditioned medium from PYCR1‐silenced BMSCs impaired oxidative phosphorylation and increased sensitivity to bortezomib.
Inge Oudaert, Lauren van den Broecke, Osman Aksoy, Judith Lind, Sonia Vallet, Arne Van der Vreken, Gamze Ates, Ann Massie, Ken Maes, Kim De Veirman, Elke De Bruyne, Karin Vanderkerken, Klaus Podar, Eline Menu   +13 more
wiley   +1 more source

ATP functions as a pathogen-associated molecular pattern to activate the E3 ubiquitin ligase RNF213

Nature Communications
The giant E3 ubiquitin ligase RNF213 is a conserved component of mammalian cell-autonomous immunity, limiting the replication of bacteria, viruses and parasites.
Juraj Ahel, Arda Balci, Victoria Faas, Daniel B. Grabarczyk, Roosa Harmo, Daniel R. Squair, Jiazhen Zhang, Elisabeth Roitinger, Frederic Lamoliatte, Sunil Mathur, Luiza Deszcz, Lillie E. Bell, Anita Lehner, Thomas L. Williams, Hanna Sowar, Anton Meinhart, Nicola T. Wood, Tim Clausen, Satpal Virdee, Adam J. Fletcher   +19 more
doaj   +1 more source

Phosphorylation of Pyruvate by the Pyruvate Kinase Reaction and Reversal of Glycolysis in a Reconstructed System

, 1959
I. Krimsky
openalex   +1 more source

Inhibition of CDK9 enhances AML cell death induced by combined venetoclax and azacitidine

Molecular Oncology, EarlyView.
The CDK9 inhibitor AZD4573 downregulates c‐MYC and MCL‐1 to induce death of cytarabine (AraC)‐resistant AML cells. This enhances VEN + AZA‐induced cell death significantly more than any combination of two of the three drugs in AraC‐resistant AML cells.
Shuangshuang Wu, Jianlei Zhao, Aaban Asfar Azmi, Avanti Gupte, Jenna Thibodeau, Shuang Liu, Jinli Yang, Guan Wang, Holly Edwards, Lisa A. Polin, Juiwanna Kushner, Sijana H. Dzinic, Kathryn White, Julie Boerner, Maik Hüttemann, Jay Yang, Yue Wang, Jeffrey W. Taub, Yubin Ge   +18 more
wiley   +1 more source